253 research outputs found
Acute Kidney Injury in Poor Countries Should No Longer Be a Death Sentence: The ISN '0 by 25' Project.
Acute kidney injury (AKI) is a common disorder throughout the world that is associated with severe morbidity, mortality and cost. Although deaths due to AKI occur in both high- and low- and middle-income countries (LMIC), the majority of avoidable deaths occur in LMIC nations. If managed adequately and in a timely fashion, the majority of these cases of AKI are preventable, treatable and often reversible with simple measures. AKI also has a major economic impact on healthcare expenditure. This is particularly true in poor countries where AKI especially impacts young productive people, imposing severe penury on their families. The International Society of Nephrology (ISN) has launched a long-term program, the '0 by 25' project, which advocates that zero people should die of untreated AKI in the poorest part of Africa, Asia and Latin America by 2025. The mission is to eventually lessen the high burden in terms of deaths consequent to this disorder in resource-poor regions worldwide. This is a challenging but potentially feasible and productive initiative that requires a broad vision about how the public and private sectors can work in partnership with the governments of the LMIC countries and leading nongovernmental organizations operating locally, to ensure sustainability of the 0 by 25 program and save many lives
Turnour necrosis factor stimulates endothelin-1 gene expression in cultured bovine endothelial cells
We have studied the effect of human recombinant tumour necrosis factor-α (TNF-α) on gene expression and production of endothelin-1 in cultured bovine aortic endothelial cells. TNF-α (10 and 100 ng ml−1) increased in a time dependent manner the preproendothelin-1 mRNA levels in respect to unstimulated endothelial cells. TNF-α induced endothelin-1 gene expression was associated with a parallel increase in the release of the corresponding peptide in the culture medium. These findings suggest that the enhanced synthesis and release of endothelin-1 occurring in conditions of increased generation of TNF, may act as a modulatory factor that counteracts the hypotensive effect and the excessive platelet aggregation and adhesion induced by TNF
Low birth weight, nephron number and chronic kidney disease
Chronic kidney diseases have a significant impact on morbidity and mortality worldwide. Low birth weight, fetal growth restriction and prematurity are indicators of fetal growth and development disorders associated with a congenital reduction in nephron number, which predisposes to an increased risk for chronic kidney disease. On an individual basis, a small nephron number at birth is not always enough to determine the onset of chronic kidney disease, but it decreases the ability of the kidneys to resist any insults to renal tissue that may occur later in life, such as exposure to nephrotoxic drugs or episodes of acute kidney injury. The high incidence of low birth weight and preterm birth globally suggests that, at the population level, the impact of alterations in fetal development on the subsequent onset of chronic kidney disease could be significant. The implementation of strategies aimed at reducing the incidence of prematurity, fetal growth restriction, as well as other conditions that lead to low birth weight and a reduced nephron number at birth, provides an opportunity to prevent the development of chronic kidney disease in adulthood. For these purposes the coordinated intervention of several specialists, including obstetricians, gynecologists, neonatologists, nephrologists, and family doctors, is necessary. Such strategies can be particularly useful in resource-poor countries, which are simultaneously burdened by maternal, fetal and child malnutrition; poor health; epidemics caused by communicable diseases; and little access to screening and primary care
Renal metabolism and urinary excretion of platelet-activating factor in the rat.
The origin of platelet-activating factor (PAF) in the urine remains ill defined. The present study documents that [3H]PAF (3.5 mu Ci) injected into the renal artery of isolated control rat kidney preparations perfused at constant pressure with a cell-free medium containing 1% bovine serum albumin (BSA) was excreted in negligible amounts (0.034%) in the urine, whereas 6% was retained by the kidney. When kidneys were perfused with a BSA-free medium, 0.029 and 71% of the total radioactivity added to the perfusate was recovered in the urine and in the renal tissue, respectively. [3H]PAF urine excretion in proteinuric kidneys from adriamycin-treated rats was still negligible (0.015%). Analysis of the renal tissue-retained radioactivity in control and proteinuric kidneys perfused with 1% BSA indicated metabolism into long chain acyl-sn-glycero-3-phosphorylcholine species, lyso-PAF, glycerols, and intact PAF. Thin layer chromatography analysis of [3H]glycerol fraction in these renal extracts showed two major components comigrating with 1-O-alkylglycerol and 1-O-alkyl-2-fatty acylglycerol. Isolated proximal tubules, but not glomeruli from nephrotic rats exposed to increasing concentrations of BSA (0-4%), had a higher PAF uptake than control tubules for BSA concentrations ranging from 0 to 0.1%. Our findings in the isolated perfused kidneys indicate that, in normal conditions, circulating PAF is excreted in the urine in negligible amounts and that the altered glomerular permeability to proteins does not affect this excretion rate. Moreover, analysis of renal tissue radioactivity documented that the renal metabolism of PAF is comparable in control and nephrotic kidneys
Chronic kidney disease and cardiovascular risk in six regions of the world (ISN-KDDC): a cross-sectional study
Background Chronic kidney disease is an important cause of global mortality and morbidity. Data for epidemiological
features of chronic kidney disease and its risk factors are limited for low-income and middle-income countries. The
International Society of Nephrology’s Kidney Disease Data Center (ISN-KDDC) aimed to assess the prevalence and
awareness of chronic kidney disease and its risk factors, and to investigate the risk of cardiovascular disease, in countries
of low and middle income.
Methods We did a cross-sectional study in 12 countries from six world regions: Bangladesh, Bolivia, Bosnia and
Herzegovina, China, Egypt, Georgia, India, Iran, Moldova, Mongolia, Nepal, and Nigeria. We analysed data from
screening programmes in these countries, matching eight general and four high-risk population cohorts collected in
the ISN-KDDC database. High-risk cohorts were individuals at risk of or with a diagnosis of either chronic kidney
disease, hypertension, diabetes, or cardiovascular disease. Participants completed a self-report questionnaire, had
their blood pressure measured, and blood and urine samples taken. We defi ned chronic kidney disease according to
modifi ed KDIGO (Kidney Disease: Improving Global Outcomes) criteria; risk of cardiovascular disease development
was estimated with the Framingham risk score.
Findings 75 058 individuals were included in the study. The prevalence of chronic kidney disease was 14·3% (95% CI
14·0–14·5) in general populations and 36·1% (34·7–37·6) in high-risk populations. Overall awareness of chronic
kidney disease was low, with 409 (6%) of 6631 individuals in general populations and 150 (10%) of 1524 participants
from high-risk populations aware they had chronic kidney disease. Moreover, in the general population,
5600 (44%) of 12 751 individuals with hypertension did not know they had the disorder, and 973 (31%) of 3130 people
with diabetes were unaware they had that disease. The number of participants at high risk of cardiovascular disease,
according to the Framingham risk score, was underestimated compared with KDIGO guidelines. For example, all
individuals with chronic kidney disease should be considered at high risk of cardiovascular disease, but the
Framingham risk score detects only 23% in the general population, and only 38% in high-risk cohorts.
Interpretation Prevalence of chronic kidney disease was high in general and high-risk populations from countries of
low and middle income. Moreover, awareness of chronic kidney disease and other non-communicable diseases was
low, and a substantial number of individuals who knew they were ill did not receive treatment. Prospective programmes
with repeat testing are needed to confi rm the diagnosis of chronic kidney disease and its risk factors. Furthermore, in
general, health-care workforces in countries of low and middle income need strengthening
ACE inhibition limits chronic injury of kidney transplant even with treatment started when lesions are established
ACE inhibition limits chronic injury of kidney transplant even with treatment started when lesions are established.BackgroundInhibition of the renin-angiotensin system (RAS) prevents development of chronic allograft dysfunction in experimental animals. Whether this therapeutic approach is effective even if started when signs of allograft nephropathy are already manifested has not been investigated.MethodsTo address this issue, we studied the effect of a late treatment with the angiotensin-convertine enzyme (ACE) inhibitor trandolapril in the Fisher 344 to Lewis rat kidney transplant model. Seven months after transplant a renal biopsy was done for graft histology examination. Thereafter rats received either no treatment (allograft-none) or trandolapril until sacrifice at month 13.ResultsAll animals were alive at the end of the study with the exception of a rat in the untreated group that died of renal insufficiency at day 292. Despite the fact that the grafts had already signs of structural injury and function impairment at the time treatment was stated, trandolapril completely restored renal function to baseline pretransplant values. Trandolapril also halted the progression of glomerular damage and suppressed intragraft T-lymphocyte infiltration and reduced the expression of the chemokine monocyte chemoattractant protein-1 (MCP-1). However, trandolapril had no direct effect on T cell function, since in vivo treatment did not modify recipient T-cell alloreactivity against donor antigens.ConclusionThese findings provide the basis for a novel treatment intervention with RAS blockade that, together with pharmacologic inhibition of the immune response, could interrupt progression of chronic allograft dysfunction and injury
Effect of Short-Term Cyclosporine Administration in Rats on Renin-Angiotensin and Thromboxane A2: Possible Relevance to the Reduction in Glomerular Filtration Rate
ABSTRACT A short-term treatment with Cyclosporin
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